Surviving the Sepsis Guidelines - NPANA · SURVIVING SEPSIS GUIDELINES 2017 TOPICS 1. Fluids 2....
Transcript of Surviving the Sepsis Guidelines - NPANA · SURVIVING SEPSIS GUIDELINES 2017 TOPICS 1. Fluids 2....
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GOLDILOCKS AND THE PANEL OF
BEARS
Surviving the Sepsis
Guidelines
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GOLDILOCKS AND THE
PANEL OF BEARS
Surviving Sepsis
Not too little….Not too much…
……..just the right amount
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MY FOCUS
• Sepsis is a HUGE topic
A. Physiology - everyone knows
macrocirulation, so my focus is
microcirculation.
B. Quick and dirty summary of the 2017
guidelines for treatment
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YOUR FOCUS
• Time is the-issue
• You will see sepsis in it’s early stages
• Post-op: bacteremia is unleashed in surgery
• Pre-op: people who have surgery tend to
have something wrong with them.
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EARLY TREATMENT
• Recognize sepsis - hypotension,
tachycardia, tachypnia, fever, malaise,
fatigue, confusion
• look for suspected source of infection
• non-specific, so not diagnostic
• Fix it while waiting for the physician
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SURVIVING SEPSIS
GUIDELINES
• Guidelines first published in 2004
• Updated in 2008, 2012 …and most recently
started revising in 2014, called the 2016
guidelines and published in 2017.
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EVIDENCE VS.
GUIDELINES• Evidence - outcomes from actual studies.
$$$, labor intensive, involves ethics and
boards, controlled numbers and types of
patients. Perfect, if you live in a fairytale,
Goldilocks.
• Guidelines - turning evidence into real world
scenarios. Done by panels of bears, none of
whom like the same thing.
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HOW GUIDELINES ARE
MADE
1. Determine the scope of guidelines
2. Selection of panel members
3. Topics and questions prioritization
4. Formulation of PICO questions and outcome
prioritization
5.Systematic review
6. Certainty of evidence assessment
7. Recommendation formulation
8. Voting on final recommendations
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MAKING GUIDELINES
• You will need a committee oversight group,
the guidelines committee groupheads, the
methodology group, the conflict of interest
chair and the panel members.
• Then all you need is 80% agreement!
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2017 GUIDELINES
We recommend the protocolized, quantitative resuscitation
of patients with sepsis- induced tissue hypoperfusion.
During the first 6 hours of resuscitation, the goals of initial
resuscitation should include all of the following as a part of a
treatment protocol:
a) CVP 8–12 mm Hg
b) MAP ≥ 65 mm Hg
c) Urine output ≥ 0.5 mL/kg/hr
d) Scvo2 ≥ 70%.
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PHYSIOLOGY OF SEPSIS
• NOT determined by a panel
• if you know physiology, you can roll with the
changing guidelines
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DEFINITION OF SEPSIS
Sepsis = life threatening organ dysfunction caused by
dysregulated host response to infection
Septic Shock = subset of sepsis with circulatory and
cellular/metabolic dysfunction associated with higher risk
of mortality
Just like life - Host response to infection is the
key!
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PHYSIOLOGY OF SEPSIS
KEY POINTS• Source of infection
• Bacteria - release endotoxin that trigger vasodilitation
and leaky capillaries
• Viral - more complicated
• Host Response
• My focus - Hypoperfusion of the macro and
microcirculation
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MACRO**CIRCULATION
• Familiar. Tangible. Visible.
• CPR, art line, BP cuff, foley catheter, Swan-
ganz catheter, vent, pulm edema, imaging
studies, rectal tube, chest tube, jp drain,
wound-vac, echo, surgery, level of alertness,
physical exam….etc.
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MACHINES THAT
MEASURE
MICROCIRCULATION
• None!
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MICRO**CIRCULATION
• Microvascular Disarray -pathogenic factors of
sepsis affects almost every cell - endothelial cells,
smooth muscle cells; white, red and plasma blood
cells; tissue cells.
• If not corrected, disarray in the microvasculature
will lead to “respiratory distress” or mitochondrial
dysfunction in tissue cells which triggers a
cascade that ends in organ destruction.
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BLOOD VESSELS
• Tone - not too little
• Flow - not too much
• Patency - clots and leaks at the same time
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ENDOTHELIUM
• Endo - inside
• Thelium - layer of cell tissue
• e.g. Onion skin
= cells that line every blood vessel in the body.
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CAPILLARIES• microcirculatory system
• blood vessels with walls that are one cell
thick.
• any inflammation or loss of tone creates a
leak
• low flow and low velocity - prone to leaking
and clotting
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MEASURING
MICRO**CIRCULATION• oxygen, CO2, lactate, SvO2, procalcitonin, CRP,
white blood cell #, H/H, electrolytes, troponin leak
- basically, send some labs.
• response of macro organs - looking for signs of
end organ dysfunction
• Goal is to treat BEFORE we reach end organ
dysfunction
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MICROVASCULAR
DISARRAY
• mitochondrial distress syndrome
= an organelle that lives in almost every cell
and makes energy
• leaky capillaries
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MIGHTY MITOCHONDRIA
MOTOR
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SURVIVING SEPSIS GUIDELINES
2017 TOPICS1. Fluids
2. Lactate
3. Vasopressors
4. Hospital based policy of response
5. Steroids
6. Blood cultures and antibiotics
7. Mechanical ventilation
8. Glucose control
9. Bicarb use
10.Transfusion goal
11.Stress ulcer prophylaxis
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EARLY TREATMENT
• Focus: #1 fluids #2 lactate and #3
vasopressors
• First line responders - you can give fluid and
pressors and affect the early
microvasculature cascade!!!!!
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TIME IS THE-ISSUE
• 2004 guidelines set the goal of treatment
within 6 hours (early goal directed therapy)
• Prevent end organ dysfunction
• Don’t wait 6 hours to address hypoperfusion!
Fix it now.
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#4 HOSPITAL BASED
POLICYTime is tissue
• Patient care and reimbursement $$$$
• Mortality rate - 20 years ago, used to be 30-50%, now it’s less
• Hospital death rate - 1 in 3 patients who die in a hospital have sepsis (says
the CDC)
• lung infection such as pneumonia 35%
• kidney or UTI 25%
• intestinal 11%
• skin 11%
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#1 FLUIDS• Pre Surviving Sepsis: levophed was “leave ‘em dead” because we did
not fluid resuscitate.
..…… too little
• 2004 - early goal directed therapy was the buzz phrase, and it
included a lot of fluid.
.…… too much
• Revisions, including 2016 - give fluid and measure their fluid
responsiveness
……..just the right amount
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#1 FLUIDS• Flow: leaky capillaries = 3rd spacing, peripheral
edema, ascites, pleural effusion, insensible losses
(emesis, sweating, fever, increased metabolic
demand) . We are losing fluid, so we need more.
• Tone: bacterial endotoxin causes vasodilitation.
Decreased tone means we need more fluid to fill the
space.
• Patency - do not want thick blood, dilute is a little
better
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#1 FLUIDS• by far the most complicated part of treating sepsis
• CVP was supposed to measure fluid status. It
doesn’t.
• Goal is to limit hypoperfusion - both macro and
micro
• SS Guideline Recs: 30cc/kg bolus over 3 hours
(about 2L)
• Dilemma - we can’t see the micro, so bring in the
lactate!
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#1 FLUID
RESPONSIVENESS• Too much? hypoxia, pulm edema, increased
work of breathing, swelling
• Too little? you have not fixed the
hypoperfusion
• Just the right amount - you fix the
hypotension, tachycardia, tachypnia, fever,
malaise, fatigue, confusion
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#2 LACTATE• a measure of hypoperfusion of the microcirculation (patient
care)
• a tangible that insurance companies can track (hospital
reimbursement)
• don’t forget our other micro measures - send the labs!
• Elevated lactate can have many causes - it is NOT diagnostic
• higher lactate does correlate with higher chance of dying
• Recs: make sure the number is decreasing
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#2 LACTATE
• to see a trend, you must have 2 points at
least! If you order one lactate, order another.
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#3 VASOPRESSORS
• 2 ways to fix hypoperfusion - fluids and
vasopressors
• according to insurance, one way to measure
it - the lactate!
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#3 VASOPRESSORS
• Tone: bacteria cause vasodilitation. Fluid alone
will not fix it.
• Flow: a large, floppy tube will have low flow -
vessels need to be filled (fluid) and pressed.
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CARDIAC OUTPUT
• Early phase of sepsis is INCREASED cardiac
output, til it wears itself out.
• Decreased output is an example of end organ
damage (we would like to prevent this with our
early treatment!)
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#3 VASOPRESSORS
• Physiology: alpha-receptors are located on blood vessels,
beta-receptors are located on heart tissue. In sepsis, you
need to increase tone (alpha) and increase cardiac output
(beta, inotrope, chronotrope).
• Vasopressors are catecholamines (flight and fight)
• Too little? you must overcome the vasodilitation response in
sepsis
• Too much? you risk catecholamine toxicity and increased
afterload
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#3 VASOPRESSORS
• Levophed/norepinephrine = alpha and beta
• Neosynephrine/phenylephrine = alpha
• Vasopressin = different mechanism, part of neurohormonal response.
Synergistic.
• Epinephrine = lots of alpha and beta (bazooka)
• Dopamine is not a pressor - it binds dopamine receptors. Dopamine
receptors are mostly on the heart and just make it go faster.
• Dobutamine is beta, so it is often helpful in the low cardiac output phase
of sepsis = later phase.
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#3 VASOPRESSORS
• Catecholamine toxicity - tachycardia, cardiac
irritability, takustubo syndrome, troponin leak
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#3 VASOPRESSORS
• Multi-modal therapy, Synergistic, limit toxicity
• Just like Hypertension - using more than one
agent to raise MAP is better
• My preference - when levophed @
10mcg/kg/min, add vasopressin
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#3 VASOPRESSORS
• MAP goal is 65.
• Bad things happen if MAP < 55.
• “Permissive hypotension” was invented by surgeons, because
patients bleed less.
• Exceptions:
• dialysis - I will tolerate MAP 60.
• chronic hypertensive - they probably need >> 65
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ANTIBIOTICS
• Antibiotics should be given within ONE hour.
• do NOT delay treatment to order a test
• However, if antibiotics are given one minute
before cultures, then the insurance
companies can FAIL you and not pay for the
entire treatment of sepsis.
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STEROIDS
• constant discussion and disagreement
• Consensus - only use them if you really have
to, i.e if all the above things aren’t working.
• Steroids are usually at least several hours
into the treatment, so should be physician
directed.
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TRANSFUSION
• Patency: capillaries are low flow, low velocity so giving thick,
cold blood is not ideal.
• Blood in a bag has little oxygen carrying capacity
• the dysfunction in sepsis is not the blood, or the lack of oxygen,
it’s the endothelium and the tissue cells.
• Historically - heparin was trialed, then Xigris to deal with micro-
clotting
• SS Guideline Recs: transfuse if Hb < 7
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BICARB
• Guidelines say ok to give if pH < 7.15
• Common sense says pH < 7 would be better
• Bandaid - short lived, no overall benefit, masks the true
acidosis which is how we measure our treatment goals
• Ok to give if you are in a pinch (it will bump the MAP while
you get pressors)
• It will cause potassium shifts and it is hypertonic 8.3%
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OTHER GUIDELINE RECS
• Mechanical Vent - use ARDSnet goal of 6ml/kr
and plateau pressure < 30
• Glucose - goal < 180.
• Stress Ulcer prophylaxis - if on the vent > 48 hrs
• DVT prophylaxis - sepsis is a high risk,
inflammatory state.
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TREATING SEPSIS1. Give fluids - not too much, not too little
• official rec - 30 cc/kg bolus over 3 hours
2. Give pressors - earlier pressors in CHF, ESRD, later pressors in drunk, dehydrated,
homeless person.
• Peripheral line is ok until you have better access- minutes, not hours!
• MAP > 65
• levophed, vasopressin
3. Track the lactate for insurance companies and as a measure of your
microcirculation
4. Time is the-issue: MAP< 55 is bad, for any time. Antibiotics within an hour!
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TREATING SEPSIS• Recall physiology - sepsis is disarray of
microvasculature system - decreased tone of
blood vessels, leaky capillaries, poor flow, poor
patency —> this is what causes the end organ
damage
• End organ damage is at the end!
• Remove the source (often not possible, unless
it’s a line infection or surgical emergency)